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. 2023 Sep 21;30(11):1640–1652. doi: 10.1038/s41594-023-01096-3

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — Model depicting the strong interplay between SSX and H2AK119ub1. SSX-C interacts with regions rich in ubiquitinated H2A on lysine K119 and therefore determines oncofusion chromatin occupancy. SSX-C binding further enhances H2AK119ub1 levels, reinforcing the presence of the SSX fusion on chromatin. Aberrant activation of Polycomb target genes is mediated by the recruitment of different transcriptional activators via their SSX-C domain.